Individual responses to active rTMS in patients with predominant negative schizophrenia may be accurately predicted using structural neuromarkers. Further multisite studies are needed to externally validate the proposed treatment stratifier and develop more personalized and biologically informed rTMS interventions.

Diabetic Retinopathy (DR) is a sight-threatening complication associated with the highly prevalent diabetes disorder. Both the microvascular damage and neurodegeneration detected in the retina caused by chronic hyperglycemia have brought special attention to Müller cells, the major macroglia of the retina that are responsible for retinal homeostasis.Given the role of glucocorticoid signaling in anti-inflammatory responses and the almost exclusive expression of glucocorticoid receptors (GR) in retinal Müller cells, administration of corticosteroid agonists as a potential treatment option has been widely studied. Although these approaches have been moderately efficacious in treating or deescalating DR pathomechanisms, there are various side effects and gaps of knowledge with regards to introducing exogenous glucocorticoids to the diseased retina. In this paper we provide a review of the literature concerning the available evidence for the role of Müller cell glucocorticoid signaling in DR and we discuss previously investigated approaches in modulating this system as possible treatment options. Furthermore, we propose a novel alternative to the available choices of treatment by using gene therapy as a tool to regulate the expression of GR in retinal Müller cells. Upregulating GR expression allows for induced glucocorticoid signaling with more enduring effects compared to injection of agonists. Hence, repetitive injections would no longer be required. Lastly, side effects of glucocorticoid therapy such as glucocorticoid resistance of GR following chronic exposure to excess ligands or agonists can be avoided.

N europathologic (1), neuroimaging (2), and cerebrospinal fluid (CSF) protein marker findings (3) indicate that vascular changes are key determinants of cognitive decline in old age. Small-vessel disease contributes to dementia cases globally, including those predominantly attributed to Alzheimer disease (AD) ( 4). An increasing number of midlife vascular risk factors are associated with a higher late-life in vivo amyloid b burden, independent from APOE (5). Vascular pathophysiology in AD is linked to toxic effects of amyloid b and hypertension-accelerated

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